Glucose-induced release of tumour necrosis factor-alpha from human placental and adipose tissues in gestational diabetes mellitus
Glucose-induced release of tumour necrosis factor-alpha from human placental and adipose tissues in gestational diabetes mellitus
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DOI：
10.1046/j.1464-5491.2001.00614.x
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发表时间：
2001-11-01
影响因子：
3.5
通讯作者：
Rice, GE
中科院分区：
文献类型：
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作者：
Coughlan, MT;Oliva, K;Rice, GE
细胞因子肿瘤坏死因子- α (tnf - α)与2型糖尿病胰岛素抵抗的发病机制有关，但与妊娠糖尿病（GDM）相关的数据有限，GDM是一种存在类似生化异常的疾病。我们研究了外源性葡萄糖对正常孕妇和GDM患者胎盘和脂肪（网膜和皮下）组织中tnf - α释放的影响。方法人组织外植体培养24 h，用ELISA法定量培养培养基中tnf - α的浓度。评估正常（5 mmol/1）和高（15和25 mmol/1）葡萄糖浓度对tnf - α释放的影响。结果6例GDM女性胎盘和皮下脂肪组织中，高糖条件下tnf - α释放量显著高于正常血糖（胎盘：25mmol /l 5915.7 +/- 2579.6和15mmol /l 4547.1 +/- 2039.1 vs. 5mmol /l 1897.1 +/- 545.5；皮下脂肪组织：25mmol /l 423.5 +/- 207.0和15mmol /l 278.5 +/- 138.7 vs. 5mmol /l 65.3 +/- 28.5 pg/mg蛋白；P < 0.05）。相反，高糖对正常孕妇（n = 6）的组织释放TNF-没有刺激作用（胎盘，25 mmol/l 1542.1 +/- 486.2和15 mmol/l 4263.3 +/- 2737.7 vs 5 mmol/1 5422.4 +/- 1599.0；皮下脂肪组织，25 mmol/l 189.8 +/- 120.4和15 mmol/l 124.5 +/- 32.3 vs 5 mmol/l 217.9 +/- 103.5 pg/mg蛋白）。这些观察结果表明，GDM患者的组织在对高葡萄糖的反应中释放了更多的tnf - α。由于tnf - α先前与糖脂代谢和胰岛素抵抗的调节有关，这些数据与tnf - α可能参与GDM发病和/或进展的假设一致。
Aims The cytokine tumour necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of insulin resistance in Type 2 diabetes mellitus, but limited data are available in relation to gestational diabetes mellitus (GDM), a disease in which similar biochemical abnormalities exist. We investigated the effect of exogenous glucose on the release of TNF-alpha from placental and adipose (omental and subcutaneous) tissue obtained from normal pregnant women, and women with GDM.Methods Human tissue explants were incubated for up to 24 h and TNF-alpha concentration in the incubation medium quantified by ELISA. The effect of normal (5 mmol/1) and high (15 and 25 mmol/1) glucose concentrations on the release of TNF-alpha was assessed.Results In placental and subcutaneous adipose tissues obtained from women with GDM (n = 6), TNF-alpha release was significantly greater under conditions of high glucose compared with normal glucose (placenta, 25 mmol/l 5915.7 +/- 2579.6 and 15 mmol/l 4547.1 +/- 2039.1 vs. 5 mmol/l 1897.1 +/- 545.5; subcutaneous adipose tissue, 25 mmol/l 423.5 +/- 207.0 and 15 mmol/l 278.5 +/- 138.7 vs. 5 mmol/l 65.3 +/- 28.5 pg/mg protein; P < 0.05). In contrast, there was no stimulatory effect of high glucose on TNF- release by tissues obtained from normal pregnant women (n = 6) (placenta, 25 mmol/l 1542.1 +/- 486.2 and 15 mmol/l 4263.3 +/- 2737.7 vs. 5 mmol/1 5422.4 +/- 1599.0; subcutaneous adipose tissue, 25 mmol/l 189.8 +/- 120.4 and 15 mmol/l 124.5 +/- 32.3 vs. 5 mmol/l 217.9 +/- 103.5 pg/mg protein).Conclusions These observations suggest that tissues from patients with GDM release greater amounts of TNF-alpha in response to high glucose. As TNF-alpha has been previously implicated in the regulation of glucose and lipid metabolism, and of insulin resistance, these data are consistent with the hypothesis that TNF-alpha may be involved in the pathogenesis and/or progression of GDM.